Furthermore, mice with cardiac-specific overexpression of mutated human αB-crystallin (hR120GCryAB) displayed increases in GSH levels and in activities of GR, glucose-6-phosphate dehydrogenase (G6PD), catalase, and GPx (indicative of reductive stress), which led to the development of cardiac hypertrophy and heart failure in these mice (77, 78). This evidence concerns the gene G6PD and cardiac hypertrophy.